Rega Institute for Medical Research

Mouse treatment

The effects of experimental treatments and genetic interventions (gene knockout) on the course of infection and pathology in murine malaria models are listed in this part of the database. For each molecule, data about the genetic background of the mouse strain (and number of backcrosses), parasite species, inoculum size (pRBC), details of the treatment/knockout, effect on parasitemia, pathology and survival, additional data of the effects of the treatments (e.g. on expression of other factors), references (Refs), and a hyperlink to the original paper in the PubMed database (U.S. National Library of Medicine, National Institutes of Health) is included.

Dynamic fields: these are the columns that you can select to show in the output table. See also "How to use MalarImDB?" for more information.

Similar precursor frequencies of CD4+ T cells able to proliferate in response to malarial antigens; CD4+ T cells were still of a predominant IFN-g (Th1) phenotype at the later stages of infection (no switch toward a IL-4 (Th2) phenotype); parasite clearance after adoptive transfer (in the chronic phase) of B cells which restores the Th2 response

Similar serum IFN-g, TNF-a, IL-10; similar serum IgG1 and IgG2a 21 days p.i.; ↓ serum IL-18 6-7 days p.i.; similar anemia and weight loss; similar production of IFN-g, IL-10 and IL-1b by splenocytes after stimulation with pRBCs

↓ weight loss at the peak of infection; ↑ serum IFN-g 5-7 days p.i., ↑ serum TNF-a and IL-10 6 days p.i. and ↑ serum IL-18 7 days p.i.; similar serum IgG1 and ↑ IgG2a 21 days p.i.; ↑ production of IFN-g, TNF-a, IL-10 and IL-1b by splenocytes after stimulation with pRBCs for 48h; similar liverpathology 10 days p.i. (serum ALT, liver necrosis and inflammation); similar pro-IL-1b mRNA expression in the spleen 6 days p.i.; ↑ caspase-1 activation in BMDMs after stimulation with pRBCs; similar IkBa and ↑Bcl-xl, cox-2 protein in the spleen 7 days p.i.;

Prolonged survival (2-3 weeks: late as well as early treatment, no effect if administered when symptoms were evident); no neurological symptoms; ↑ protection when administered i.v. compared to i.p.; similar mononuclear cell sequestration in the brain (WT: sequestering cells are almost all monocytes or mononuclear phagocytes, only very few T, B cells or neutrophils were observed)

Prolonged survival (2-3 weeks: late as well as early treatment, no effect if administered when symptoms are evident); no neurological symptoms; ↓ serum TNF-a; similar mononuclear cell sequestration in the brain

Prolonged survival (2-3 weeks: late as well as early treatment); no neurological symptoms; no vascular permeability in brain and ↓vascular permeability in lungs; ↓ mononuclear cell sequestration in brain and lungs; ↓ (brain) and similar (lungs) platelet accumulation; similar microhemorrhages in the brain; ↓ myeloperoxidase activity (neutrophil enzyme) in lungs; similar liver pathology; ↓injected aggregated albumin localization in brain and lungs

Less severe weight loss and hypothermia; ↓ serum levels (in vivo) and production of IFN-g and TNF-a by splenocytes (in vitro); TNF-a serum levels and production by splenocytes remained elevated 4 weeks p.i.

similar results as with anti-CD25 treatment 1 day before infection (see above), thus the protective effect is probably mediated by natural Treg cells and not by inducible Treg cells (although the latter might contribute as well)